Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 102, Issue 46, Pages 16789-16794Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0507718102
Keywords
genomic; vascular progenitor cell; aging; inflammation; bone marrow obsolescence
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Funding
- NHLBI NIH HHS [P01 HL073042, R01 HL071536, HL073042, HL71536] Funding Source: Medline
- NIA NIH HHS [R01 AG023073, P60 AG011268] Funding Source: Medline
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Atherosclerosis is a chronic inflammatory process and progresses through characteristic morphologic stages. We have shown previously that chronically injecting bone-marrow-derived vascular progenitor cells can effect arterial repair. This repair capacity depends on the age of the injected marrow cells, suggesting a progressive decline in progenitor cell function. We hypothesized that the progression of atherosclerosis coincides with the deteriorating repair capacity of the bone marrow. Here, we ascribe patterns of gene expression that accurately and reproducibly identify specific disease states in murine atherosclerosis. We then use these expression patterns to determine the point in the disease process at which the repair of arteries by competent bone marrow cells ceases to be efficient. We show that the loss of the molecular signature for competent repair is concurrent with the initiation of atherosclerotic lesions. This work provides a previously unreported comprehensive molecular data set using broad-based analysis that links the loss of successful repair with the progression of a chronic illness.
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